A review and summary of the contents of biophysical reviews volume 8, 2016

Remedios, Cris dos

doi:10.1007/s12551-017-0249-7

Cited by 4 publications

(3 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This pro-inflammatory environment may activate fibroblast proliferation and excessive production of extracellular matrix proteins which correlates with cardiomyopathies ( West et al, 2011 ; Lin and Kerkelä, 2020 ). These alterations at molecular levels are associated with cellular changes such as hypertrophy, fibrosis, accumulation of misfolded proteins, loss of cardiac cells, extracellular matrix remodeling and amyloid deposition and structural changes in the myocardium like left ventricle hypertrophy and left auricle hypertrophy, which causes diastolic dysfunction ( Steenman and Lande, 2017 ; Liang and Gustafsson, 2020 ). It has also been reported that mtDNA and whole mitochondria are released into bloodstream which offers a new biomarker of mitochondrial function and stress.…”

Section: Cardiac Mitochondria In Agingmentioning

confidence: 99%

mtDNA Heteroplasmy at the Core of Aging-Associated Heart Failure. An Integrative View of OXPHOS and Mitochondrial Life Cycle in Cardiac Mitochondrial Physiology

Elorza

Soffia

2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

The most common aging-associated diseases are cardiovascular diseases which affect 40% of elderly people. Elderly people are prone to suffer aging-associated diseases which are not only related to health and medical cost but also to labor, household productivity and mortality cost. Aging is becoming a world problem and it is estimated that 21.8% of global population will be older than 65 years old in 2050; and for the first time in human history, there will be more elderly people than children. It is well accepted that the origin of aging-associated cardiovascular diseases is mitochondrial dysfunction. Mitochondria have their own genome (mtDNA) that is circular, double-stranded, and 16,569 bp long in humans. There are between 500 to 6000 mtDNA copies per cell which are tissue-specific. As a by-product of ATP production, reactive oxygen species (ROS) are generated which damage proteins, lipids, and mtDNA. ROS-mutated mtDNA co-existing with wild type mtDNA is called mtDNA heteroplasmy. The progressive increase in mtDNA heteroplasmy causes progressive mitochondrial dysfunction leading to a loss in their bioenergetic capacity, disruption in the balance of mitochondrial fusion and fission events (mitochondrial dynamics, MtDy) and decreased mitophagy. This failure in mitochondrial physiology leads to the accumulation of depolarized and ROS-generating mitochondria. Thus, besides attenuated ATP production, dysfunctional mitochondria interfere with proper cellular metabolism and signaling pathways in cardiac cells, contributing to the development of aging-associated cardiovascular diseases. In this context, there is a growing interest to enhance mitochondrial function by decreasing mtDNA heteroplasmy. Reduction in mtDNA heteroplasmy is associated with increased mitophagy, proper MtDy balance and mitochondrial biogenesis; and those processes can delay the onset or progression of cardiovascular diseases. This has led to the development of mitochondrial therapies based on the application of nutritional, pharmacological and genetic treatments. Those seeking to have a positive impact on mtDNA integrity, mitochondrial biogenesis, dynamics and mitophagy in old and sick hearts. This review covers the current knowledge of mitochondrial physiopathology in aging, how disruption of OXPHOS or mitochondrial life cycle alter mtDNA and cardiac cell function; and novel mitochondrial therapies to protect and rescue our heart from cardiovascular diseases.

show abstract

Section: Cardiac Mitochondria In Agingmentioning

confidence: 99%

mtDNA Heteroplasmy at the Core of Aging-Associated Heart Failure. An Integrative View of OXPHOS and Mitochondrial Life Cycle in Cardiac Mitochondrial Physiology

Elorza

Soffia

2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…All these imaging modes can provide nanometric spatial resolution images of cells or single proteins in fluid conditions [ 19 ]. The development of high-speed atomic force microscopy (HS-AFM), rapid imaging, and real-time visualization offered the advantage of analyzing the dynamic behavior of biological macromolecules [ 20 ]. So far, the current performance of HS-AFM reported is to record movies of molecular motion with up to 15 Hz frame rate, without disturbing the biomolecular functions.…”

Section: Afm and Snom: The Use Of Force And Lightmentioning

confidence: 99%

Scanning Probe Microscopies: Imaging and Biomechanics in Reproductive Medicine Research

Andolfi

Battistella

Zanetti

et al. 2021

IJMS

View full text Add to dashboard Cite

Basic and translational research in reproductive medicine can provide new insights with the application of scanning probe microscopies, such as atomic force microscopy (AFM) and scanning near-field optical microscopy (SNOM). These microscopies, which provide images with spatial resolution well beyond the optical resolution limit, enable users to achieve detailed descriptions of cell topography, inner cellular structure organization, and arrangements of single or cluster membrane proteins. A peculiar characteristic of AFM operating in force spectroscopy mode is its inherent ability to measure the interaction forces between single proteins or cells, and to quantify the mechanical properties (i.e., elasticity, viscoelasticity, and viscosity) of cells and tissues. The knowledge of the cell ultrastructure, the macromolecule organization, the protein dynamics, the investigation of biological interaction forces, and the quantification of biomechanical features can be essential clues for identifying the molecular mechanisms that govern responses in living cells. This review highlights the main findings achieved by the use of AFM and SNOM in assisted reproductive research, such as the description of gamete morphology; the quantification of mechanical properties of gametes; the role of forces in embryo development; the significance of investigating single-molecule interaction forces; the characterization of disorders of the reproductive system; and the visualization of molecular organization. New perspectives of analysis opened up by applying these techniques and the translational impacts on reproductive medicine are discussed.

show abstract

“…Also, insulin treatment activates the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin (PI3K-Akt- mTOR) kinase pathway and increase the expression level of the N2B isoform with the presence of RBM20 [ 57 ]. Even though the precise role of RBM20 in the hormone-induced change in titin splicing is still not clear, these findings provide novel insights into developing therapeutic agents targeting RBM20 to induce titin isoform switching for treatment of heart disease [ 59 ].…”

Section: Rbm20-dependent Alternative Splicing Mechanismmentioning

confidence: 99%

Muscle-Specific Mis-Splicing and Heart Disease Exemplified by RBM20

Rexiati

Sun

Guo

2018

Genes

View full text Add to dashboard Cite

Alternative splicing is an essential post-transcriptional process to generate multiple functional RNAs or proteins from a single transcript. Progress in RNA biology has led to a better understanding of muscle-specific RNA splicing in heart disease. The recent discovery of the muscle-specific splicing factor RNA-binding motif 20 (RBM20) not only provided great insights into the general alternative splicing mechanism but also demonstrated molecular mechanism of how this splicing factor is associated with dilated cardiomyopathy. Here, we review our current knowledge of muscle-specific splicing factors and heart disease, with an emphasis on RBM20 and its targets, RBM20-dependent alternative splicing mechanism, RBM20 disease origin in induced Pluripotent Stem Cells (iPSCs), and RBM20 mutations in dilated cardiomyopathy. In the end, we will discuss the multifunctional role of RBM20 and manipulation of RBM20 as a potential therapeutic target for heart disease.

show abstract

A review and summary of the contents of biophysical reviews volume 8, 2016

Cited by 4 publications

References 52 publications

mtDNA Heteroplasmy at the Core of Aging-Associated Heart Failure. An Integrative View of OXPHOS and Mitochondrial Life Cycle in Cardiac Mitochondrial Physiology

mtDNA Heteroplasmy at the Core of Aging-Associated Heart Failure. An Integrative View of OXPHOS and Mitochondrial Life Cycle in Cardiac Mitochondrial Physiology

Scanning Probe Microscopies: Imaging and Biomechanics in Reproductive Medicine Research

Muscle-Specific Mis-Splicing and Heart Disease Exemplified by RBM20

Contact Info

Product

Resources

About